For 2nd year B.Sc Nursing students

1. ANEMIA
Presented By:
Mr. Nandish.S
Asso. Professor
Mandya Institute of Nursing Sciences

3. DEFINITION
 It is a deficiency in number of erythrocytes, the quantity of
hemoglobin or the volume of packed RBC’s.
 It is a condition in which the hemoglobin concentration is lower than
normal.
 It is a condition that develops when your blood produces lower than
normal amount of healthy red blood cells.
 It is a blood disorder in which the blood has a reduced ability to carry
oxygen due to lower number of RBC or reduction in the amount of
hemoglobin.

5. INCIDENCE & PREVALENCE :
 It is one of the major killer disease in India.
 Research reveals that every second Indian women is anemic.
 One in every menstrual deaths is directly due to anemia.
 It affects both adults and children of both sex.
 Pregnant women & Adolescent girls are more susceptible to this
disease.

6. ETIOLOGIC CLASSIFICATION OFANEMIA
1. Decreased Erythrocyte Production
2. Blood loss
3. Increased Erythrocyte Destruction
MORPHOLOGIC CLASSIFICATION OFANEMIA
1. Normocytic Normochromic (Normal size & color)
2. Macrocytic Normochromic ( Large size & normal color)
3. Microcytic Hypochromic (Small size & pale color)

7. Decreased Erythrocyte Production
Decreased Hemoglobin Synthesis • Iron deficiency
• Thalassemia (Decreased Globin
synthesis)
• Sideroblastic anemia (decreased
porphyrin)
Defective DNA Synthesis • Vitamin B12 deficiency
• Folic Acid deficiency
Decreased Number of Erythrocyte
Precursors
• Aplastic Anemia
• Anemia of leukemia
• Chronic Diseases
Chemotherapy

8. Blood Loss
Acute  Trauma
 Blood vessel rupture
 Persistent Hematuria
Chronic  Gastritis
 Menstrual Flow / Menorrhagia
 Regular blood Donors
 Hemorrhoids

9. Increased Erythrocyte
Destruction
Intrinsic  Abnormal Hemoglobin (Sickle Cell
Anemia)
 Enzyme Deficiency (G6PD)
 Membrane abnormalities
Extrinsic  Physical Trauma
 Antibodies (Autoimmune)
 Infectious Agents & Toxins

10. Based on the severity of Signs & Symptoms :
1. Mild
• Hemoglobin : 10 to 14 gm/dl
• Palpitation
• Exertional Dyspnea
2. Moderate
• Hemoglobin : 6 to10 gm/dl
• Dyspnea
• Increased Palpitation
• Fatigue
Continued ………………

11. 3. Severe :
• Hemoglobin : less than 6 gm/dl.
• Pallor, pruritus
• Icteric Conjunctiva, Blurred vision
• Glossitis, Smooth tongue
• Tachycardia, Murmur
• Tachypnea, Orthopnea, Dyspnea at rest
• Headache, Vertigo, irritability, Depression
• Anorexia, Dysphagia, Sore mouth, Hepato-splenomegaly
• Bone pain
• Weight loss, Lethargy, Sensitivity to cold.

12. IRON DEFICIENCY ANEMIA :
DEFINITION :
It is defined as anemia associated with either inadequate absorption or
excessive loss of iron from the body.

13. Etiology :
 Inadequate dietary intake.
 Malabsorption
- After gastro intestinal surgery.
- Malabsorption syndrome
 Blood loss
- Chronic blood loss from GI (Peptic Ulcer, Gastritis, Esophagitis,
Hemorrhoids) & GU System (Menstrual bleeding)
- At the time of Delivery & Lactation
 Pregnancy (diversion of iron towards fetus)
 Dialysis treatment

14. CLINICAL FEATURES :
• Fatigability
• Dizziness
• Irritability
• Headache
• Palpitation
• Glossitis
• Stomatitis
• Dry pale skin
• Spoon shaped nails
• Hair loss

15. DIAGNOSTIC STUDIES :
- History collection & Physical Examination
- Stool examination : for presence of occult blood
- Endoscopy or colonoscopy : to detect GI Bleeding.
- Blood examination :
• decreased Hemoglobin / RBC / Hematocrit
• Decreased or normal WBC
• Decreased or normal Platelets.

16. MANAGEMENT :
1. Parenteral Iron therapy :
It is initiated during
- Malabsorption
- Intolerance to oral replacement (colitis)
- Needs in excess amount that cannot be given through oral route.
- Poor compliance patients & Hemodialysis patients.
 Iron is given either intramuscularly or intravenously.
 IM – given deep IM in the upper & outer quadrant of buttocks using
18 or 20 gauze needle.
 Iron Dextran or Iron sucrose contains 50 mg/dl. It is diluted while
administration to patients. Test dose is given to rule out any allergy.

17. 2. Oral therapy
- Oral Iron & Folic acid tablets are usually prescribed.
- Total daily dosage : 150 – 200 mg elemental iron.
- Give iron in divided dose. ( each dose of 50 – 100 mg)
- Taking Iron with vitamin C, enhances its absorption.
- Iron preparations cause stool to become dark due to excess excretion
of iron.
- Constipation is common, hence stool softners can be advised.

18. 3. Others :
- Advise the patient to consume Liver, muscle meat, Egg, Dry fruits,
Legumes, Dark green leafy vegetables, bread, cereals, pototoes, etc..
- Encourage to include fibre rich diet to handle constipation.
- If iron deficiency is from acute blood loss, it require transfusion of
packed RBC.
- Hemoglobin returns to normal by 2 – 4 months.
- Replacement therapy is prolonged to 6 – 12 months if ongoing
bleeding is present.

19. MEGALOBLASTIC ANEMIA :
 They are the group of disorders caused by impaired DNA Synthesis
and characterized by presence of large RBC.
 When DNA synthesis is impaired, it results in defective RBC
Maturation.
 Megaloblast represent large and abnormal RBC’s.
 They are easily destroyed because they have fragile cell membrane.
 Two common forms of Megaloblastic anemia are : Cobalamin
Deficiency & Foloic Acid deficiency.

20. COBALAMIN DEFICIENCY ANEMIA :
 Intrinsic Factor (IF) is required for absorption of Cobalamin, which is
secreted by parietal cells of gastric mucosa.
 Pernicious Anemia is a disease of insidious onset, caused by an
absence of Intrinsic Factor from gastric mucosal atrophy or
Autoimmune destruction of Parietal cells.
 The main cause for cobalamin deficiency is Pernicious anemia.
 Pernicious Anemia is usually seen in middle aged people (after 40
years).

21. Etiology :
1. Inborn errors of cobalamin metabolism.
2. Erythroleukemia
3. Malabsorption
• Inadequate production of Intrinsic Factor
- Pernicious Anemia
- Gastrectomy (Partial or Total)
• Inadequate releasing of Vitamin B12 from blood
- Abnormal Stomach functioning, Chronic pancreatic Insufficiency
• Terminal ileum disease (Celiac disease, Crohn’s disease)
• Others (bacterial overgrowth, intestinal obstruction)
Continued …..

22. 4. Inadequate intake
- Pure vegetarians
5. Medications
- Neomycin
- Nitrous oxide
- Long term use of H2 receptor blockers

23. CLINICAL FEATURES :
GI Manifestations Neurologic Manifestations
Atrophic Glossitis / sore tongue Abnormal gait , Symmetric
Neuropathy
Weight loss Numbness & weakness
Anorexia Parasthesia
Abdominal pain Memory loss
Nausea & vomiting Spasticity & incontinence

24. DIAGNOSTIC STUDIES :
History collection & Physical Examination
Blood examination
- Macrocytic anemia
- Leukopenia
- Thrombocytopenia
- Decreased reticulocyte count
Bone marrow examination
It reveals hypercellular changes, abnormal large megaloblasts with
nuclear cytoplasmic asynchrony.
 Schilling Test : a medical investigation used to evaluate vitamin B12
absorption. Usually result will be positive for this type of anemia.

25. TREATMENT :
- Increasing dietary cobalamin will not correct anemia, if any impaired
absorption is there in Ileum.
- However, patient is instructed on adequate dietary intake to maintain
good nutrition.
- Parenteral administration of cobalamin (Cyanocobalamin) is the
treatment of choice.
- Dosage & frequency may vary. A typical treatment schedule consists of
1000mg of cobalamin (IM) daily for 2 weeks, then weekly once until
hematocrit is normal and then monthly once for lifetime.
- A nasal gel is also available (Nascobal).
- As long as supplemental cobalamin is used, anemia can be reversed.

27. FOLIC ACID DEFICIENCY ANEMIA
 Folic acid is needed for DNA synthesis leading to RBC formation &
maturation.
 Food supply folic acid : Spinach, Asparagus, Brocolli, Beans, Peanuts,
Liver, Aquatic foods, sunflower seeds, etc.
 Banana rich in folate can meet daily needs when they are combined
with other folic acid foods.
 It is absorbed in Duodenum of small intestine.

28. ETIOLOGY :
 Poor nutrition / Inadequate intake : green leafy vegetables, citrus
fruits, Yeast, dreid beans, nuts & grains
 Malabsorption syndromes : small intestine disorders.
 Alcohol abuse / Excessive alcoholism
 Medications that affect absorption of Folic Acid : Methotrexate, Oral
contraceptives, Anti seizure drugs.
 Hemodialysis
 Pregnancy & Lactation and during Infancy.
 Malignancy

29. CLINICAL MANIFESTATIONS :
 Clinical features during Folic acid deficiency are similar to those of
cobalamin deficiency except neurologic problems.
 GI disturbance include dyspepsia & smooth beefy red tongue.

30. DIAGNOSTIC STUDIES :
 History collection & Physical Examination
 Decreased Hemoglobin level
 Decreased Serum Folate level
 Gastric analysis : positive for HCl.

31. TREATMENT :
 Encourage the patients to consume foods rich in Folic acid.
 Replacement therapy : oral dose is 1mg / day & in malabsorption upto
5mg can be administered.
 The duration of treatment depends on cause.

32. APLASTIC ANEMIA
A rare condition in which body fails to produce sufficient new blood
cells.
It is a syndrome of bone marrow failure characterized by peripheral
pancytopenia & bone marrow hypoplasia.
It is a severe, non cancerous, hematologic condition in which body
fails to make enough blood cells.

33. ETIOLOGY :
The causative factors can be divided into two major groups.
Congenital : chromosomal alterations.
- Fanconi syndrome (A disease of proximal renal tubule in which
glucose, uric acid & amino acids are not absorbed properly.
- Congenital Dyskeratosis
- Amegakaryocytic thrombocytopenia
Acquired : it results from
- Exposure to Ionizing Radiation, chemical agents (Benzene)
- Viral & Bacterial infections (Hepatitis)
- Medications (Antimetabolites, Alkylating agents, Antiseizure drugs)
- Idiopathic (more than 70% cases)

34. Clinical Manifestations :
General : Fatigue, Dyspnea, weight loss
Neurologic : Headache, Vertigo, Irritability, Depression
Cardiovascular : Tachycardia, Neutropenia, Cardiac murmur
Susceptible to infection, Febrile
Thrombocytopenia can lead to Petechiae, Ecchymosis, Epistaxis

35. Diagnostic Studies :
History collection & Physical Examination
Decreased Hemoglobin, WBC & platelets
Low Reticulocyte count
Prolonged Bleeding time
Elevated serum iron & Total Iron Binding capacity (TIBC)
Bone marrow examination : dry tap – marrow is hypocellular with
increased yellow marrow (fat content).

36. Treatment :
Prognosis of untreated anemia is very poor (75% fatal).
It is based on identifying & removing the causative agent and
providing the supportive care.
Bone marrow transplantation.
Immunosuppressive therapy with Anti Thymocyte Globulin (ATG) &
Cyclosporine. ATG is a horse serum that contains polyclonal
antibodies against human T Cells. This therapy is partially beneficial
& avoids transfusion.

37. SICKLE CELL DISEASE
Sickle Cell Disease is a group of inherited, autosomal recessive
disease characterized by the presence of abnormal form of
Hemoglobin in the Erythrocyte.
It is a group of disorder that cause red blood cells to become
mishappen and break down.
It is a genetic disorder in which red blood cells bend out into a sickle
shape.

38. In this condition, the abnormal hemoglobin (HbS) causes the
erythrocyte to stiffen & elongate taking on a sickle shape.
It results from substitution of Valine for glutamic acid on β globin
chain of Hemoglobin on Chromosome 11.
Sickle cell disease is identified during infancy or early childhood.
It is an incurable disease.
It is commonly seen in African americans, 1 in 350 to 500 live births.

39. Types of Sickle Cell Disease :
1. Sickle cell Anemia
2. Sickle cell – Thalassemia
3. Sickle cell – HbC disease
4. Sickle Cell Trait

40. 1. Sickle Cell Anemia
It is the most severe form.
It occurs when a person is Homozygous for Hemoglobin S, The
person has inherited HbS from both parents.
2 & 3. Sickle cell – Thalassemia & Sickle cell – HbC disease
It occurs when a person inherits Hb S from one parent & another type
of abnormal Hemoglobin (such as Thalassemia or Hb C) from another
parent.
Both the above forms are not common & are less severe.

41. 4. Sickle Cell Trait
It occurs when a person is Heterozygous for Hemoglobin S, the
person has inherited Hemoglobin S from one parent & normal
Hemoglobin from the other parent.
It is typically a very mild to asymptomatic condition.

43. Clinical Manifestations :
Pallor
Decreased activity tolerance
Jaundice
Primary symptom is pain, which is severe and affects back, chest,
extremities and abdomen.
Damaged vision : the sickled blood cells affect the blood vessels that
connect to retina, causing optimal damage.
Limited Growth : the scarcity of oxygen caused by sickled cell
anemia is detrimental to healthy human growth.

44. Diagnostic Studies :
History collection & Physical examination
Peripheral blood smear
Sickling test
Electrophoresis
X – Ray (preferably long bones)
Doppler studies
MRI

45. Complications :
SYSTEM DISEASE CONDITIONS
Respiratory system Pneumonia, Pulmonary Hypertension,
Acute Chest syndrome
Cardio Vascular system Myocardial Infarction, Congestive Heart
failure, corpulmonale
Opthalmic Retinal Hemorrhage, scarring &
detachment, blindness,
Musculo – Skeletal system Osteoporosis, Osteosclerosis
Neurologic Cerebro vascular accident
Others Renal failure, chronic leg ulcers, Priapism

46. MANAGEMENT :
No specific treatment for this disease.
Treatment mainly focuses on alleviating the symptoms & minimizing
the end stage organ damage.
Instruct to avoid high altitude, maintain adequate fluid intake and
treat infections promptly.
If leg ulcers are present, treat them with adequate bed rest, antibiotics,
warm saline soak, mechanical debridement and grafting.
Acute chest syndrome treated with broad spectrum antibiotics,
oxygen administration & fluid therapy.
Continued ……………….

47. MANAGEMENT :
Oxygen therapy
Fluid therapy / administration
Transfusion therapy
Pain management
Anti Sickling agents (Hydroxy urea)

48. ANEMIA DUE TO BLOOD LOSS :
It can be occurred due to
 Acute blood loss
 Chronic blood loss
Etiology :
 Trauma
 Complications of Surgery
 Conditions or diseases that disrupt vascular integrity

49. CLINICAL MANIFESTATIONS :
Volume lost 10% : No identified features or display of symptoms.
Volume lost 20% : No detectable signs or symptoms at rest.
Tachycardia with exercise & mild postural hypotension.
Volume lost 30% : Postural hypotension & Tachycardia at exercise.
Volume lost 40% : Blood pressure, Central venous pressure & cardiac
output below normal at rest, Rapid thready pulse,
cold & calmy skin.
Volume lost 50% & above : potential shock & death.
Internal hemorrhage causes pain in abdomen.

50. MANAGEMENT :
IV Fluids : Dextran, Albumin, Hetastarch and Crystalloid electrolyte
solutions like Ringer’s Lactate, etc..
Blood Transfusion (packed RBC) may be needed, if the blood loss is
significant.
If the bleeding is related to platelet or clotting disorder, replacement of
the deficiency is addressed.
Supplemental Iron is prescribed on regular basis.

51. NURSING MANAGEMENT :
1. Impaired tissue perfusion related to decreased cellular components
required for the delivery of Oxygen to the cells.
2. Activity intolerance related to weakness, imbalance between oxygen
supply and demand.
3. Imbalanced nutrition, less than body requirement related to poor
nutritional intake, failure to digest or absorb food necessary for the
formation of blood cells.
4. Hypoxemia related to decreased hemoglobin.
5. High risk for infection related to inadequate secondary defence
(Leukopenia).
6. Ineffective therapeutic regimen management related to lack of
knowledge, exposure & inadequate interpretation of information.